acute pancreatitis

1. ACUTE PANCREATITIS
By:
Dr.NANDHINI

2. ETIOLOGY
 GALL STONES (30% - 60%)
 ALCOHOL(15% - 30%)
 POST ERCP (5% - 10%)
 POST TRAUMATIC (1%)
 DRUGS
 POST OPERATIVE

3. DRUGS
1.Azathioprine 8.Dapsone
2. 6MP 9.INH
3.Asparginase 10.Metronidazole
4.Pentamidine 11. estrogens
5.Didanosine 12.Tamoxifen
6.Valproate 13.Corticosteroids
7.Tetracyclines 14.ACE (-)tors
15. Thiazides

4.  Vascular causes & Vasculitis
 CTD
 Carcinoma head of pancreas
 Infections
Bacterial: mycoplasma, MAC,
Campylobactor, leigionella, Lptospirosis.
Viral: Mumps,Rubella,Varicella,
Coxsackie ,CMV,echo virus.
Parasites: Ascaris, Clonorchis )

5.  Auto immune (type 1&2)
 Scorpion bite
 Malnutrition
 Peritoneal dialysis etc….

6. If recurrent episodes…….
 Metabolic : hypertriglyceridemia,
hypercalcaemia
 Pancreatic divisum
 IPMN
 Heriditary Pancreatitis
 Cystic fibrosis
 Drugs
 Idiopathic

7. PATHOGENESIS
MOST ACEPTED THEORY ---
AUTO DIGESTION
PHASES
1. Enzyme Autoactivation
2.Chemoattraction & sequestration ofPMN and
macrophages releasing CK
3. Local & Systemic effects

9. TRYPSIN
Other Proenzyme activation
Autoactivation
Prophospholipase Pro elastase prekallikrein
Phospholipase elastase kallikrein
Fat necrosis weakens BV clotting .
cascade
HEMORRHAGE

10. Others……
Genetic :
 1. PRSS1(cationictrypsinogengene)
 2.SPINK1(pancreaticsecretorytrypsininhibitor)
 3.CFTR
 4.CTRC(chymotrypsinreceptor gene)
 5.CASR(calciumsensingreceptorgene)
Hypertriglyceridaemia
Hypercalcaemia
Drugs

11. Enzyme activation mechanisms
 Pancreatic duct obstruction
 Primary acinar cell injury
 Defective intracellular transport of Enzymes
Leucocyte sequestration
 Releases chemokines like IL-1ß ,IL-6, TNF, PAF,
SubstanceP.
 Sustains injury
Local and sytemic effects

12. CLINICAL PRESENTATION

13.  Epigastric pain (D/D)
 Nausea,Vomiting
 Abdominal distension
 Cool perpheries
 Blindness (may be transient)
 Respiratory distress
 Hiccoughs

14.  Mild Icterus
 Signs of shock
 SIRS
 Cullens sign
 Grey turners sign
 Fox sign
 Erythematous tender skin nodules
 Evidence of pleural effusion
 Guarding and rigidity
 Sluggish bowel sounds

16. Fox sign

17. Mechanism

18.  Other obsolete signs :
Korte sign
Kamenchick sign
Mayo robsons sign

19. DIAGNOSIS
2 of these 3criteria
 Typical abdominal pain
 3 fold or more raise in serum Amylase or Lipase
 CT findings s/o accute Pancreatitis

20. REVISED ATLANTA
CLASSIFICATION

21. ACUTE PANCREATITIS
Interstitial Necrotising
Acute peripancreatic Acute Necrotic
Fluid collection Collection
after 4wks
Pseudocyst Walled of
Necrosis

22. MORPHOLOGICAL FEATURES
1. INTERSTITIAL PANCREATITIS
 No necrosis
 Diffuse enhancement

23. 2.ACCUTE PANCREATIC FLUID COLLECTION
(APFC)
 no necrosis
 Peri pancreatic fluid <4wks duration
 No encapsulation
 No intra pancreatic extension

24. 3.Pancreatic pseudocyst
 No necrosis
 >4wks duration
 Well encapsulated
 Homogenous fluid density

25. 4. ACUTE NECROTISING PANCREATITIS
 Parenchymal
or
peri pancreatic necrosis

26. 5.ANC (Acute Necrotic Colletion)
 Necrotic areas
 Heterogenous areas
 Intra or peri pancreatic extension
 Non encapsulated

27. 6.WON(Walled Of Necrosis)
 Necrotic areas
 >4wks duration
 Heterogenic fluid collection
 Well encapsulated
 Intra or peri pancreatic collection

28. SEVERITY
ASSESSMENT

29.  Assessing injury to other organs
1. SOFA score
2. Modified Marshall Scoring System

30. Assessing severity of Pancreatitis
1. BISAP score
2.Ransons score
3. Glasgow score
4. APACHE-II score
5. CT severity Index
6. Modified CT severity Index
7.HAPS score
8.Revised Atlanta Classification

31. SOFA SCORE
Assesses 6 systems i.e,
respiratory
cardiovascular
renal
hepatic
coagulation
neurological

34. MODIFIED MARSHALLSCORING SYSTEM

35. BISAP score
 B – BUN > 22mg%
 I - Impaired mental status
 S - SIRS (Any 2 of 4 criteria)
 A - Age >60 yrs
 P -Pleural effusion

36. RANSON’S score
On Admission With in 48 hrs of
admission WBC >
16,OOOcells/cumm
 AGE >55yrs
 Glucose >200mg/dl
 LDH > 350 IU/L
 AST > 250U/L
 PCV fall > 10%
 Arterial Po2 < 60mm
Hg
 BUN raise > 5mg%
 Calcium < 8 mg/dl
 Base Deficit >
4mEq/L
 Fluidsequestration >
6lit

37. RANSONS SCORE
 11 point scoring system
POINTS ------ MORTALITY
0-2 - 0%
3-4 - 15%
5-6 - 50%
>6 - 70%

38. GLASGOW SCALE
On admission With in 48 hrs
 WBC > 15,000
cells/cumm
 Age > 55yrs
 Glucose > 200
mg/dl
 Arterial Po2 <60
mmHg
 Urea >45 mg/dl
 S.Calcium <8mg/dl
 S.Albumin
<3.2mg/dl
 S.LDH >600U/L
 S.ALT > 200 U/L

39. APACHE – II scoring system
 12 point scoring system
 After 24 hrs of admission into ICU

40. CTSI
 Includes
BALTHAZAR SCORE
&
NECROSIS SCORE

41. BALTHAZAR SCORE
GRADE --- DESCRIPTION --- SCORE
A Normal pancreas 0
B Enlarged pancreas 1
C Inflammatorychanges 2
in pancreas
and peri pancreatic fat
D Ill defined single 3
peripancreatic fluid collection
E ≥2 Ill defined fluid collections 4

42. NECROSIS SCORE
% --- SCORE
NONE 0
≤30% 2
30-50% 4
>50% 6

44. Grading
 0-2 : Mild
 4-6 : Moderate
 8-10 : severe

45. HAPS (Harmless Acute Pancreatitis
Score)
 High PPV
 Used to predict a milder course of illness
 Includes 1.Guarding &/ Rebound
tenderness +/-
2.Creatinine <2mg/dl
3.Hematocrit < 43%(M)
<39.6%(F)
 Score of “0” good prognosis

46. ATLANTA CLASSIFICATION
 MILD : no local complications & organ failure
 MODERATELY SEVERE : transient organ failure
<48hrs +/- local complications
 SEVERE : persistent organ failure (>48hrs) with
local and systemic complications

47. GRADING OF SEVERITY OF
ATTACK
 BISAP score of 3 - 5
 Ransons’ score ≥ 3
 Glassgow score ≥ 3
 APACHE II score ≥ 8
 CTSI (Balthazar) ≥ 6
 Modified CTSI score of 8-10
 Persistent organ failure(RevisedAtlanta)
 CRP >150mg/dl

48. Lab parameters……….
*CBP * Hematocrit
* S. Amylase * BUN
* S. lipase * S.Creatinine
* S. Calcium * CRP
* S. Triglycerides * LFT
*S. Trypsin * Coagulation
* Blood sugar profile

49. ENZYMES
 S.Amylase
 Normal values 23-85U/L
 Sources : parotids, pancreas, fallopian tube,
sweat,
 Types : S-type and P-type (isoenzymes)
 Metabolism : renal & hepatic
 Half life : 7 to 14 hrs
 sensitive & Highly nonspecific

50.  High Amylase levels seen in
*Pancreatic disorders
*Salivary disorders
*Renal failure
*Macroamylasemia
*Intestinal diseases- gut infarction
perforation ,peritonitis,obstruction
* Ruptured ectopic pregnancy
* ectopic production : cancers of pancreas,
thymus, breast, lung ,ovary.
* DKA and other acidotic conditions

51. Amylase
 No corelation b/n severity of pancreatitis and
degree of enzyme elevation
 Usually rises within 24hrs of attack and returns
to normal within 48-72hrs
 After 3-7 days normalises even if inflammation
continues.
 Hence normal levels doesn’t exclude the disease


52.  Amylase – P more specific than serum Amylase

53. Low Amylase levels…………..
 May be seen in
certain pancreatic cancers
Toxaemia of pregnancy

54. Confirmed Pancreatitis with Normal
Amylase levels…..
 Hypertriglyceridemia
(high triglycerides interferes with enzyme assay)
 Some times in patients with Alcoholic pancreatitis

55. S.Lipase
 More specific (95%)
 Remains for longer time in serum than amylase
 Stays even upto 8to 14 days
 useful in patiets who are presenting lately
 Half life about 10to 14hrs
 Level of lipase can’t predict disease severity and
outcome

56.  High serum lipase levels seen in
*Hollow viscus perforation
*Intestinal obstruction
*Intestinal ischemia
 In case of Alcoholic pancreatitis
S. lipase is more elevated than S.Amylase

57. S.CALCIUM
 May be high or low
 Hypercalcemia – cause
 Hypocalcemia - effect of pancreatitis
 Low Calcium levels correlates with severity of
disease
 <7mg/dl with normal albumin levels associated
with tetany have poor prognosis

58. S. TRIGLYCERIDES
 High levels of >900-1000 mg/dl associated with
increased risk
 Estimated in fasting states
 Usually asso. with
Type I ,V Hyperlipidemias

59. Markers of Hemoconcentration
*BUN > 22 mg/dl
*Hematocrit atAdmission >44 %(highNPV)
*S.Creatinine at 48 hrs of Admission
> 1.8mg/dl (high PPV)
 Helpful in assessing fluid status of patient
 Predictors of Pancreatic Necrosis

60.  CRP
Elevated CRP of >150 mg/dl at 48 hrs of
admission suggestive of severe disease.
single important prognostic indicator of severity
 LFT
hyperbilirubinemia >4mg/dl may be seen in 10%
patients assiciated with gall stone associated
pancreatitis
Elevated ALP also seen

61. IMAGING
IN
PANCREATITIS

62. ROLE OF PLAIN X-RAY

63. SIGNS
 Sentinal loop
 Colon cutoff sign
 Renal halo sign
 Loss of psoas shadow
 Gall stone may be seen
 Multiple calcifications in case of accute on chronic
pancreatitis patient
 pleural effusion Lt>Rt

64. COLON CUTOFF SIGN

65.  D/D for Colon Cut Off sign
*Pancreatitis
*IBD
*Mesenteric ischemia
*Carcinoma Colon

66. SENTINAL LOOP SIGN D/D

68. ROLE OF
USG AND DOPPLER

70.  Diffuse Decrease in Pancreatic Echogenicity
(than liver)
 Free fluid
 Increased volume of Pancreas i.e, Bulky Pancreas
(AP diameter >24mm)
 Gall stones
 Parenchymal inhomogenicty may correlate with
necrosis
 Pseudocysts
 Spleenic vien thrombosis etc..

71. ROLE OF CT IN PANCREATITIS

72. MANAGEMENT

73. 1.FLUID RECUSCITATION
 Main stay of therapy
 Initially 15-20ml/kg bolus administered
 Then f/b 3ml/kg/hr infusion should be kept to
maintain urine output of >0.5cc/kg/hr
 Serial evaluations done to assess fluid status
clinically and by measuring BUN & Hematocrit
every 8-12 hrs.

74.  Decrease in serial BUN & Hematocrit ensues
adequate resuscitation
 Adjust fluid rates of infusion in patients with co
morbid cardiac , pulmonary , renal illnesses
 Increasing BUN & Hematocrit inspite of
aggressive fluid therapy can be treated with
repeated volume challenge with 2L crystalloid
bolus f/b increase in infusion rate by 1.5ml/kg/hr
.

75.  If still unresponsive transfer to intensive unit for
careful hemodynamic monitering.
 Fluid of choice is Lactated Ringer which reduces
systemic inflammation and preffered over Normal
Saline

76. 2. Pain Management
 Opiates like Buprenorphine is DOC
 Pethidine can be given alternatively
 Meperidine 100to 150mg IM can be given every
4th hrly if necessary
 NSAID of choice is Metimazole
 Morphine is contraindicated.

77. 3.NBM
 NPO is no longer advisable
 Usually kept for 2-3 days with ryles tube
aspiration
 As soon as possible oral fluids are allowed even
enzymes are elevated
 Initially with soft liquids
 Later with low fat diet preferred
 Maintains barrier integrity and decreases
bacterial translocation

78. 4. Role of Antibiotics
 Prophylactic therapy has no role
 Mild disease doesn’t needs antibiotics at all
 For severe pancreatitis i.e, with necrosis may
benefit
 Definitive role is seen with proven cases of
infected Necrosis
 Antibiotics of choice are CARBAPENUMS

79.  IMIPENUM 5oomg 8th hrly given
 Alternatively Cefuroxime 1.5g IV TID
f/b 250mg oral BD for 14 days
 Meropenum and
combination of Ciprofloxacin and Metronidazole
doesn’t appear to reduce frequency of infected
necrosis and MODS

80. 5.Supportive therapy
 FFP transfusions in case of DIC
 Ionotropes for cardiac support
 Mechanical ventilation for ARDS
 Hemofilteration etc….

81. In Spl situations like……
 1. Gall stone pancreatitis :
*should undergo ERCP within
24-48hrs of admission to prevent
recurrence
*cholecystectomy may be done on
later date

82.  2.Hypertriglyceridemia :
*Initially treated with Insulin ,
Heparin, plasmapheresis
* later hypolipidemic drugs like
Fibrates , Niacin can be used.
 3. ERCP induced Pancreatitis:
*Rectal Indomethacin , Allopurinol ,
newer drug Ulinastatin , aggressive
hydration with ringered lactate can
prevent this .

83. COMPLICATIONS

84. SYSTEMIC LOCAL
 Pleural effusion
 ARDS
 Atelectasis
 Hypotension
 arrythmias
 Pericardial effusion
 DIC
 ATN
 Renal vein /artery thrombosis
 Hyperglycemia
 Encephalopathy
 Purtscher’s retinopathy
 Subcutaneous fat necrosis
 Acute fluid collection
 Necrosis
(sterile/infected)
 Pseudocyts
 Pancreatic abscess
 Portal / spleenic vein
thrombosis
 Pseudoaneurysm

85. PURTSCHER’S RETINOPATHY

86. NECROSIS
 May be sterile(60%) or
infected(40%)
 Prophylactic antibiotics no role
 Infected necrosis can be suspected by clinical
deterioration with persistant MODS
 Aspirated under CT guidance sent for gram’s and
culture

87. Pseudocyst
 Emperical antibiotic therapy with Imipenum can
be started
 Step up approach
 Requires 4wks for epithelisation and maturation
 Resolve spontaneously with in 6wks
 May or may not communicate with ductal system

88. SURGEON’S ROLE
 1. Necrosis - necrosectomy
*indications :
worsening sepsis in case of
infected necrosis
 2.pseudocyst –
>6cm lasting for 12 wks producing
pressure symptoms warrants
surgery

90. Prognosis
 Risk of chronic pancreatitis after an attack of
accute alcoholic pancreatitis
is 13% in 10 yrs
& 16% in 20 yrs

91. Follow up care
 Aimed towards assessment of risk of
DM
Exocrine Pancreatic insufficiency
etc..

92. THANK U